This article is from March 2007 and may contain outdated material.
Vitreous hemorrhage has an incidence of seven cases per 100,000, which makes it one of the most common causes of acutely or subacutely decreased vision. Although the diagnosis of vitreous hemorrhage is generally straightforward, management is dictated by uncovering the underlying etiology.
The vitreous humor is 99 percent water. The remaining 1 percent is made up of collagen and hyaluronic acid, giving it a gelatinous consistency and optical clarity. The vitreous body is defined by the internal limiting membrane of the retina posterolaterally, by the nonpigmented epithelium of the ciliary body anterolaterally, and by the posterior lens capsule and lens zonular fibers anteriorly. This space represents 80 percent of the eye and has a volume of approximately 4 ml. The vitreous is firmly attached to the retina in three places: the strongest attachment is anteriorly at the vitreous base, followed by the optic nerve head and retinal vasculature.
Mechanisms of Hemorrhage
The mechanisms of vitreous hemorrhage fall into three main categories: abnormal vessels that are prone to bleeding, normal vessels that rupture under stress, or extension of blood from an adjacent source. (See “Mechanisms of Vitreous Hemorrhage.”)
Abnormal vessels. Abnormal retinal blood vessels are typically the result of neovascularization due to ischemia in diseases such as diabetic retinopathy, sickle cell retinopathy, retinal vein occlusion, retinopathy of prematurity or ocular ischemic syndrome. As the retina experiences inadequate oxygen supply, vascular endothelial growth factor (VEGF) and other chemotactic factors induce neovascularization. These newly formed vessels lack endothelial tight junctions, which predispose them to spontaneous bleeding. They also coexist with a fibrous component that often contracts, putting additional stress on already fragile vessels. Also, normal vitreous traction with eye movement can lead to rupture of these vessels.
Rupture of normal vessels. Normal vessels can rupture when sufficient mechanical force overcomes the structural integrity of the vessel. During a posterior vitreous detachment, vitreous traction on the retinal vasculature may compromise a blood vessel, especially at the firm attachments mentioned above. This may happen with or without a retinal tear or detachment. However, vitreous hemorrhage in the setting of an acute symptomatic posterior vitreous detachment should alert the clinician that the risk of a concurrent retinal break is quite high (70–95 percent).
Blunt or perforating trauma can injure intact vessels directly and is the leading cause of vitreous hemorrhage in people younger than 40.
A rare cause of vitreous hemorrhage is Terson’s syndrome, which refers to an extravasation of blood into the vitreous due to a subarachnoid hemorrhage. The blood is not an extension of the subarachnoid hemorrhage. Rather the sudden increase in intracranial pressure can cause retinal venules to rupture.
Blood from an adjacent source. Pathology adjacent to the vitreous can also cause vitreous hemorrhage. Hemorrhage from retinal macroaneurysms, tumors and choroidal neovascularization can all extend through the internal limiting membrane into the vitreous.
Signs and Symptoms
The symptoms of vitreous hemorrhage are varied but usually include painless unilateral floaters and/or visual loss. Early or mild hemorrhage may be described as floaters, cobwebs, haze, shadows or a red hue. More significant hemorrhage limits visual acuity and visual fields or can cause scotomas. Patients often say vision is worse in the morning as blood has settled to the back of the eye, covering the macula.
Patients should be questioned regarding a history of trauma, ocular surgery, diabetes, sickle cell anemia, leukemia, carotid artery disease and high myopia.
Complete examination consists of indirect ophthalmoscopy with scleral depression, gonioscopy to evaluate neovascularization of the angle, IOP and B-scan ultrasonography if complete view of the posterior pole is obscured by blood. Dilated examination of the contralateral eye can help provide clues to the etiology of the vitreous hemorrhage, such as proliferative diabetic retinopathy.
The presence of vitreous hemorrhage is not hard to detect. At the slit lamp, red blood cells may be seen just posterior to the lens with the slit beam set “off-axis” and the microscope on the highest power. In nondispersed hemorrhage, a view to the retina may be possible and the location and source of the vitreous hemorrhage may be determined. Vitreous hemorrhage present in the subhyaloid space is also known as preretinal hemorrhage. Such a hemorrhage is often boat-shaped as it is trapped in the potential space between the posterior hyaloid and the internal limiting membrane, and settles out like a hyphema. Dispersed vitreous hemorrhage into the body of vitreous has no defined border and can range from a few small distinct red blood cells to total obscuration of the posterior pole.
The blood is typically cleared from within the vitreous hemorrhage at a rate of approximately 1 percent per day. Blood outside the formed vitreous resolves more quickly. Vitreous hemorrhage is cleared more quickly in syneretic and vitrectomized eyes, and more slowly in younger eyes with well-formed vitreous. The natural history of vitreous hemorrhage depends on the underlying etiology with the worst prognoses for diabetics and AMD patients.
With the exception of proliferative vitreoretinopathy, complications of vitreous hemorrhage typically occur if blood has been present for more than one year.
Hemosiderosis bulbi is a serious complication thought to be caused by iron toxicity as hemoglobin is broken down. Since hemolysis occurs slowly, the iron-binding capacity of proteins in the vitreous usually outpaces the slow rate of hemolysis, thereby avoiding hemosiderosis bulbi.
Proliferative vitreoretinopathy. After vitreous hemorrhage, proliferative vitreoretinopathy can occur. It is thought that macrophages and chemotactic factors induce fibrovascular proliferation, which can lead to scarring and subsequent retinal detachment.
Ghost cell glaucoma. Ghost cells are spherical, rigid, khaki-colored red blood cells filled with denatured hemoglobin present in long-standing vitreous hemorrhage. If these cells gain access to the anterior chamber, their shape and rigidity can block the trabecular meshwork, resulting in ghost cell glaucoma.
Hemolytic glaucoma. In hemolytic glaucoma, free hemoglobin, hemoglobin-laden macrophages and red-blood cell debris can block the trabecular meshwork.
The presence of a retinal detachment may be determined using ultrasonography if an adequate view of the posterior segment is not possible. Vitrectomy is performed urgently when a retinal detachment or break is identified. Provided the retina is attached, observation is on an outpatient basis. If the view to the posterior pole is blocked, limitation of activities and elevation of the head of the bed while sleeping may allow the blood to settle inferiorly and permit visualization of the superior retina where retinal breaks most commonly occur. Retinal breaks are sealed with cryotherapy or laser photocoagulation. If a retinal detachment has been ruled out, patients may return to normal activities.
Once the retina can be visualized, treatment is aimed at the underlying etiology as soon as possible. If neovascularization from proliferative retinopathy is the cause, laser panretinal photocoagulation is performed, if possible through the residual hemorrhage, to cause regression of neovascularization. A krypton laser may aid photocoagulation as it passes through hemorrhage better than argon lasers. An indirect laser system may also allow energy delivery to the retina around a vitreous hemorrhage. Alternatively, in the interim, intravitreal anti-VEGF agents may induce regression of the neovascularization until laser photocoagulation is possible.
Vitrectomy is also indicated for nonclearing vitreous hemorrhage, neovascularization of the iris and/or angle, or ghost cell glaucoma. Timing of vitrectomy depends on the underlying etiology.
New therapies, such as intravitreal injection of hyaluronidase, are currently being studied and may provide additional treatment options in the future.
Mechanisms of Vitreous Hemorrhage
Diabetic retinopathy (31–54 percent of vitreous hemorrhages are caused by diabetes)
Neovascularization from branch or central retinal vein occlusion (4–16 percent)
Sickle cell retinopathy (0.2–6 percent)
Rupture of Normal Vessels
Retinal tear (11–44 percent)
Trauma (12–19 percent)
Posterior vitreous detachment with retinal vascular tear (4–12 percent)
Retinal detachment (7–10 percent)
Terson’s syndrome (0.5–1 percent)
Blood From Adjacent Source
Macroaneurysm (0.6–7 percent)
Age-related macular degeneration (0.6–4 percent)
Source: Spraul, C. W. and H. E. Grossniklaus, Surv Ophthalmol 1997;42(1):3–39.
Patients should be followed periodically to monitor for clearing of the vitreous hemorrhage. If the patient has systemic disease, such as diabetes, follow-up with a primary care provider should also be recommended. If an adequate view to the posterior pole is not possible, patients should be reevaluated every two or three weeks with B-scan ultrasonagraphy to exclude a retinal break or detachment. In the event of recurrent vitreous hemorrhage, referral to a retinal specialist for possible vitrectomy is warranted.
Timing of Vitrectomy
|Iris or angle neovascularization
|Type 1 diabetes
|Subhyaloid vitreous hemorrhage
|Type 2 diabetes
||two or three months
||three months or more
Anticoagulation of any type (e.g., aspirin, warfarin, clopidogrel) has not been identified as a risk factor for the development of a vitreous hemorrhage. The Early Treatment Diabetic Retinopathy Study1 indicated that aspirin did not worsen vitreous hemorrhage, thus aspirin and other forms of anticoagulation are generally not discontinued after the development of a vitreous hemorrhage.
1 Ophthalmology 1991;98(5 Suppl):741–756.
Dr. Berdahl is a resident, and Dr. Mruthyunjaya is an assistant professor of ophthalmology. Both are at Duke University.